Nitric Oxide Involved in the Leptin Effect on Food Intake in Broiler and Leghorn Chickens
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Experiments were conducted to evaluate nitric oxide (NO) involvement in the leptin effect on food intake in both broiler and Leghorn chickens. The first experiment studied the effect of leptin combined with L-arginine on the food intake in broilers. Intracerebroventricular (ICV) administration of human recombinant leptin injection decreased (P=.01) food intake from 15 to 150 minutes compared to the control group treated with artificial cerebrospinal fluid ( aCSF) while food intake was increased by L-arginine. Food intake between the group receiving leptin and L-arginine was similar to the control group. Therefore, broilers were sensitive to the anoregenic effects of leptin, while L-arginine, a NO precursor appeared to attenuate the leptin effect on food intake. The effect of leptin and L-NNA on food intake in broilers was measured in the second experiment. Lepin, L-NNA and leptin plus L-NNA decreased food intake. The NO inhibitor L-NNA tended to enhance the suppression of leptin on food intake. In the third experiment, using Leghorns instead of broilers, the ICV injection of leptin decreased food intake from 15 to 60 minutes postinjection (P=.05). However, food intake was not affected by injection of L-arginine plus leptin. Therefore, L-arginine appeared to antagonize the leptin inhibitory effect on food intake. A small increase food intake induced by L-arginine was also observed (P=.09). The change of food intake in Leghorns administered leptin and L-NNA were measured in Experiment 4. Food intake was decreased by L-NNA and leptin with the effects lasting 60 minutes, similar to that observed in broilers (P<0.0l). For group B (leptin treatment), there was decreased food intake within 45 minutes (P=.04) and the effect disappeared 60 minutes, post injection. Also, the results along with Experiment 2 demonstrated that NO mediated the effect of leptin in Leghorns. The fifth experiment investigated the change in concentration of metabolites of nitric oxide after injection of leptin within 30 minutes. The group treated with the leptin had a lower level of metabolites of nitric oxide in the hypothalamus than the control group (P=.004). This effect further demonstrates that leptin modulated feeding activity through its inhibition on nNOS activity in the hypothalamus. These results showed that both leptin and NO participated in the regulation of food intake in broiler and Leghorn chickens, and the effect of hypothalamic neuropeptidergic circuitry leptin on food intake was mediated by NO.
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